Prolonged Carbon Monoxide Exposure Research Articles

Effectiveness of Hyperbaric Oxygenation Versus Normobaric Oxygenation Therapy in Carbon Monoxide Poisoning: A Systematic Review.

Carbon monoxide (CO) is a gas product of combustion, considered highly poisonous. Prolonged CO exposure is responsible for more than half of fatal poisonings and is also one of the leading causes of poisoning in Western countries.We aimed to compare the effectiveness of therapy with hyperbaric oxygen (HBO) versus normobaric oxygen (NBO) in the setting of carbon monoxide poisoning (COP). We independently searched the National Library of Medicine’s Medline (PubMed™), ScienceDirect™, and Scielo™ for any relevant studies published from 1989 to 2017, using the following keywords: hyperbaric therapy, hyperbaric oxygenation, normobaric therapy, carbon monoxide poisoning, carboxyhemoglobin, Haldane effect. We analyzed the studies that suggested the effectiveness of HBO or NBO. Also, we searched for studies related to COP; including history, epidemiology (risk factors, incidence, demographics), pathophysiology, clinical manifestations, diagnosis, and treatment.Sixty-eight articles were found, sixteen of which dealt with either HBO or NBO or both. Twelve suggested HBO as the treatment of choice in COP; four studies indicated that NBO was an adequate treatment due to its cost-effectiveness and availability in the emergency department (ED).HBO has been shown in several studies to be effective in moderate to high-risk COP situations, being the therapy of choice to avoid sequelae, especially neurologically. NBO can be considered as a reasonable alternative due to its cost-effectiveness. The availability and understanding of different therapeutic interventions are critical in the management of patients with COP in ED and the Critical Care unit.

Risk factors for the delayed onset of neuropsychologic sequelae following carbon monoxide poisoning.

AimCarbon monoxide (CO) poisoning often manifests delayed neuropsychological sequelae. The risks and preventive factors for the development of delayed neuropsychological sequelae are controversial at present. The purpose of this retrospective study was to assess the risk factors for this condition.MethodWe studied 81 patients with CO poisoning admitted to the Critical Care and Emergency Medicine Center at the Kansai Medical University from 2006 to 2012. All patients (64 males and 17 females; average age, 45.9 years) were divided into non‐ delayed neuropsychological sequelae and delayed neuropsychological sequelae groups and retrospectively studied. Patient data were analyzed by univariate and multivariate analyses.ResultsThe results of our study indicated that prolonged CO exposure, elevated serum creatinine phosphokinase levels, head image abnormality in the basal ganglion or white matter region, low Glasgow Coma Scale score, bedsore occurrence, and CO poisoning attributable to burning charcoal were each predictive risk factors for the development of delayed neuropsychological sequelae. Bedsore occurrence and serum creatinine phosphokinase elevation were significant risk factors by multivariate analysis, whereas no significant differences were found for age, gender, mean blood pressure, heart rate, arterial carboxyhemoglobin and lactate concentrations, or base excess.ConclusionWe identified several predictive risk factors of delayed neuropsychological sequelae. We believe that these factors will contribute to identifying optimum therapeutic methods and follow‐up terms for patients with acute CO poisoning at risk of developing delayed neuropsychological sequelae.

Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury

Myocardial damages due to ischemia-reperfusion (I/R) are recognized to be the result of a complex interplay between genetic and environmental factors. Epidemiological studies suggested that, among environmental factors, carbon monoxide (CO) urban pollution can be linked to cardiac diseases and mortality. The aim of this work was to evaluate the impact of exposure to CO pollution on cardiac sensitivity to I/R. Regional myocardial I/R was performed on isolated perfused hearts from rats exposed for 4 wk to air enriched with CO (30-100 ppm). Functional variables, reperfusion ventricular arrhythmias (VA) and cellular damages (infarct size, lactate dehydrogenase release) were assessed. Sarcomere length shortening and Ca(2+) handling were evaluated in intact isolated cardiomyocytes during a cellular anoxia-reoxygenation protocol. The major results show that prolonged CO exposure worsens myocardial I/R injuries, resulting in increased severity of postischemic VA, impaired recovery of myocardial function, and increased infarct size (60 +/- 5 vs. 33 +/- 2% of ischemic zone). The aggravating effects of CO exposure on I/R could be explained by a reduced myocardial enzymatic antioxidant status (superoxide dismutase -45%; glutathione peroxidase -49%) associated with impaired intracellular Ca(2+) handling. In conclusion, our results are consistent with the idea that chronic CO pollution dramatically increases the severity of myocardial I/R injuries.

Whole body oxygen consumption and critical oxygen delivery in response to prolonged and severe carbon monoxide poisoning

Background: Carbon monoxide (CO) poisoning remains the leading cause of death by poisoning in the world. One of the major proposed mechanisms for CO toxicity is the binding of CO to cytochrome oxidase and interference with cellular oxygen utilization but evidence for this is inconclusive. Aim of study: This study examined the effects of prolonged CO exposure on the dynamics of whole body oxygen consumption (VO 2) and oxygen delivery (DO 2) in an attempt to observe if CO exposure results in a defect of oxygen utilization defect as determined by a reduction in VO 2 during the course of poisoning prior to reaching the point where VO 2 is directly dependent on DO 2. This critical level of DO 2 (DO 2crit) produced by CO poisoning was compared to historical values produced by other insults, which decrease global body DO 2. Methods: Five small dogs were ventilated for 2 h with 0.25% CO and room air followed by 0.5% CO until death. Cardiac index ( Q), DO 2, VO 2, oxygen extraction ratio (OER), and systemic lactate were measured every 15 min until death. Results: Carboxyhemoglobin (COHb) levels increased linearly over 2.5 h to values above 80% until death. VO 2 remained constant and not significantly different from baseline below a COHb of 80%. At COHb levels above 80%, VO 2 precipitously dropped. Similarly lactate levels were not significantly elevated from baseline until VO 2 dropped. DO 2 decreased by 78% (from 23±6 ml/kg/min to 5±4 ml/kg/min) over time despite an increase in Q by 58% until levels of COHb were above 80%. OER increased from 19±5% to 50±11% until death. The calculated DO 2crit was 10.7±4 ml/min/kg, which is not significantly different from values ranging from 7 to 13 ml/min/kg reported in the literature due to other insults, which reduce DO 2. Conclusion: In this canine model of prolonged CO exposure, no gradual reduction in VO 2 or increase in systemic lactate prior to reaching DO 2crit was noted. In addition, CO exposure does not appear to change the DO 2crit. The combination of these findings does not support the theory that CO produces a whole body intracellular defect in oxygen utilization.

Cardiodynamic changes during prolonged carbon monoxide exposure in the rat

Adult male rats were exposed to 500 ppm CO (38–42% COHb) for periods of time from 1–42 days. Hematocrit rose gradually from 49.8 to 69.7%. Cardiomegaly developed as reported earlier. Using an open chest anesthetized preparation, stroke index, mean stroke power, and mean cardiac output were seen to increase sharply upon initial CO exposure and to remain elevated for the duration of exposure. Concurrently, both total systemic resistance and total pulmonary resistance fell sharply and remained depressed. Left ventricle (LV) and right ventricle (RV) systolic pressures and mean aortic pressure rose modestly, but nonsignificantly over the first 14 days of exposure, declining somewhat thereafter. The maximum rate of change of LV pressure ( dP dt ) tended to rise above control values during the first 2 weeks of exposure. There was no consistent change in heart rate. Enhanced cardiac output via increased stroke volume is seen as a compensatory mechanism to provide adequate tissue oxygen delivery during CO intoxication. The greater continuous heart work involved may be the major factor responsible for development of CO-induced cardiomegaly.

Influence of Prolonged Carbon Monoxide Exposure and Altitude Hypoxia on Serum Lipids in Man

Influence of Prolonged Carbon Monoxide Exposure and Altitude Hypoxia on Serum Lipids in Man

Oxygen Affinity and Acid-Base Status of Human Blood during Exposure to Hypoxia and Carbon Monoxide

In eight subjects exposed to hypoxia at high altitude the oxyhemoglobin dissociation curve was shifted to the right, the half saturation oxygen tension at pH 7.40 being changed from 26.7 to 30.2 mm Hg on the average. The decreased affinity of hemoglobin for oxygen appeared within 12 hours after exposure to hypoxia. The shift was confirmed in short exposure experiments using simulated high altitude in a low pressure chamber. At prolonged carbon monoxide exposure the expected shift of the oxygen dissociation curve to the left occurred, but no adaptive changes were found. The physiological implication of these differences are discussed. It is suggested that the rapid shift to the right at high altitude may be a physiological regulation.

Influence of Prolonged Carbon Monoxide Exposure and High Altitude on the Composition of Blood and Urine in Man

The influence of exposure to carbon monoxide [average carboxyhaemoglobin saturation 13 per cent) and high altitude (3.454 m) on a number of compounds in blood and urine was investigated in 8 healthy volunteers for 8 and 10 days respectively. Reticulocyte counts increased 2–3 fold; moderate increases were seen in the urinary volume, on an average 400–800 ml/24 hrs. Compared to the remaining days of the study significantly higher amounts of sodium, chloride and calcium were excreted on the first day of exposure to both forms of hypoxia.

Influence of Prolonged Carbon Monoxide Exposure and Altitude Hypoxia on Serum Lipids in Man

Serum lipid levels were investigated in 8 young volunteers exposed to carbon monoxide (average carboxyhaemoglobin saturation 13 per cent) and to an altitude of 3.454 m for 8 and 10 days respectively. Small, but significant increases were seen in serum cholesterol levels during carbon monoxide exposure as well as at high altitude. It is suggested that this effect of hypoxia is due to an inhibition of lipoprotein lipase.

Influence of Prolonged Carbon Monoxide Exposure and High Altitude on the Composition of Blood and Urine in Man

Influence of Prolonged Carbon Monoxide Exposure and High Altitude on the Composition of Blood and Urine in Man